OEDEMA

Dr FONJE Ahmed
 OUTLINE
• Oedema: definition, pathophysiology, and causes
• Common causes:
Heart failure
Nephrotic syndrome
Cirrhosis
Premenstrual edema and pregnancy
Drug-induced edema
Cerebral oedema
• Approach to a patient presenting with oedema
• Management of oedema
• Case senario
 CASE
• Mr.A.B., a 68 years old man, was admitted to the hospital. He
suffers from fatigue, shortness of breath on exertion, cough,
tenderness in the right upper quadrant of the abdomen and
ankle swelling.

• On examination, he was pale and his hands were cold, his

temperature was 37C, pulse 130 beats per minute and
irregular. His jugular venous was elevated and pitting edema
was present in both feet and ankles. Crepitations were
present over the lung bases. There was enlargement of the
liver beyond the costal margin that was tender.
• Questions?

• What is the most likely diagnosis??

• What is the cause of hepatomegaly in this
patient??
• In a chest x-ray, what do you expect to see??
• What is the type of edema he have??
 CASE 2
• A 72-year-old man goes to his GP complaining of painless swelling
of both legs since 2 months ago. The swelling started at the ankles
but now his legs, and thighs are swollen. His face is puffy in the
mornings on getting up. His weight is up by about 10 kg over the
previous 3 months.
• He has noticed that his urine appears to be frothy in the toilet. He
has noted gradual increasing shortness of breath, but denies any
chest pain. He has also developed spontaneous bruising over the
past 6 months.
• He had HTN diagnosed 13 years ago, and MI 4 years previously. He
continues to smoke 30 cigarettes a day, and drinks about 30 units
of alcohol a week. His medication consists of atenolol 50 mg once
a day.
 Definition
• It may be defined as abnormal and excessive
accumulation of “free fluid” in the interstitial tissue
spaces and serous cavities.
• •Free fluid in body cavities
• –Ascites: peritoneal cavity
• –Hydrothorax or pleural effusion: pleural cavity
• –Hydropericardiumor pericardial effusion: pericardial
cavity
• •Free fluid in interstitial space: space between the
cells
 Types
Classification
1) According to pathophysiological mechanism:
a) Transudate (low protein content)
b) Exudate (high protein content)

2) According to location:
a) Localized
b) Generalized

3) According to clinical finding:

a) Pitting
b) Non-pitting.
Examples
Localised: Venous edema, Lymphatic edema,
allergy/agioedema, inflammation
Generalised: Cardiac edema, Hepatic edema,Renal
edema, Endocrine edema
Pitting: due to cardiac & renal causes, liver disease,
calcium channel blockers, early stage of filiarisis
Non-pitting: Myxoedema, Elephantiasis,
Angioneurotic
 Pathophysiology
• Generation of interstitial fluid is regulated by the forces of the
Starling equation.
• Hydrostatic pressure within blood vessels tends to cause water to
filter out into the tissue.
• This leads to a difference in protein concentration between blood
plasma and tissue.
• As a result the oncotic pressure of the higher level of protein in the
plasma tends to draw water back into the blood vessels from the
tissue.
• Starling's equation states that the rate of leakage of fluid is
determined by the difference between the two forces and also by
the permeability of the vessel wall to water, which determines the
rate of flow for a given force imbalance.
• Decreased plasma oncotic pressure.
• Increased capillary hydrostatic pressure
• Lymphatic obstruction.
• Inflammation ( inc oncotic pressure of interstitial fluid, and
decreased tissue tension).
• Increased capillary permeability.
• Sodium and water retention.
 1. Reduced Plasma Oncotic
Pressure
• Reduced albumin synthesis in liver/ Protein
malnutrition

• Fall in plasma oncotic pressure

• Net movement of fluid into interstitial tissues

• OEDEMA
• The examples of oedema by this mechanisms are seen
in the following conditions

• Oedema of renal disease e.g. in nephrotic

syndrome, acute glomerulonephritis

• Ascites of liver disease e.g. in cirrhosis.

• Oedema due to other causes of hypoproteinaemia

e.g. in protein-losing enteropathy.
 2. Increased Hydrostatic
Pressure
• Rise in hydrostatic pressure at the venular end
of capillaries to a level more than plasma
oncotic pressure

• Minimal/No Reabsorption of fluid at venular

end

• OEDEMA
• The examples of oedema by this mechanisms are
seen in the following disorders
• Oedema of cardiac disease e.g. in congestive
cardiac failure, constrictive pericarditis.
• Ascites of liver disease e.g. in cirrhosis of liver.
• Passive congestion e.g. in mechanical obstruction
due to thrombosis of veins of the lower legs,
varicosities, pressure by pregnant uterus, tumors et.
• Postural oedema e.g. transient oedema of feet and
ankles due to increased venous pressure seen in
individuals who remain standing erect for longtime
such as traffic constables.
 3. Lymphatic Obstruction
• Impaired lymphatic drainage

• Localised LymphOEDEMA
• Radial mastectomy for Ca breast
• Pressure on main lymph ducts
• Inflammation of lymphatics
• Occlusion of Lymphatics by malignant cells
• Milroy’s disease
 4. Inflammation
Capillary endothelial injury by toxins/ histamine/ anoxia/
drugs

Endothelial gap

Increased capillary permeability to plasma protein

Decreased plasma oncotic pressure

OEDEMA
5. Increased capillary permeability
• As described previously, an intact capillary endothelium is a
semipermeable membrane which permits the free flow of water
and crystalloids but allows minimal passage of plasma proteins
normally.

• However, when the capillary endothelium is injured by various

'capillary poisons' such as toxins and their products, histamine,
anoxia, venoms, certain drugs and chemicals, the capillary
permeability to plasma proteins is enhanced due to development
of gaps between the endothelial cells.

• This, in turn, causes reduced plasma oncotic pressure and elevated

oncotic pressure of interstitial fluid which consequently produces
oedema.
• The examples of oedema by this mechanism are seen in the
following conditions

• Generalized oedema due to increased vascular permeability

may occur in systemic infections, poisonings, certain drugs
and chemicals, anaphylactic reactions and anoxia.

• Localized oedema such as

- Inflammatory oedema as seen in infections, allergic reactions,
insect-bite, irritant drugs and chemicals. It is generally exudate
in nature.
- Angioneurotic oedema is an acute attack of localized oedema
occurring on the skin of face and trunk and may involve lips,
larynx, pharynx and lungs. It is possibly neurogenic or allergic
in origin.
 Sodium and Water
Retention
Hypovolaemia

Renal Vasoconstriction Renin ADH

GFR Aldosterone Reabsorption of water

Renal retention of Na and water

OEDEMA
• The examples of oedema by these mechanisms are
as under

• Oedema of cardiac disease e.g. in congestive

cardiac failure.

• Ascites of liver disease e.g. in cirrhosis of liver

• Oedema of renal disease e.g. in nephrotic syndrome,

glomerulonephritis.
 Most common causes of
Generalized oedema
• Heart failure
• Cirrhosis
• Nephrotic syndrome and other forms of renal
disease
• Premenstrual oedema and pregnancy

• Cerebral oedema(Localised)
 Left Heart failure oedema
Volume and
Left Heart EDV pressure in Pressure in LA
Failure LV

Leakage of fluid Hydrostatic P Pulmonary

into interstitial exceeded pressure
space Oncotic P

Pulmonary
oedema
 Clinical features of
Pulmonary oedema
• Shortness of breath and orthopnea.
• Chest pain in case of MI
• O/E: tachypneic, diaphoretic patient with wet
rales and possibly a diastolic gallop (S3) and
heart murmurs.
• The diagnosis of pulmonary edema should be
confirmed by radiologic studies.
• Pulmonary edema in a "butterfly distribution“ due to left
ventricular failure. Chest radiograph shows large perihilar
opacities in patient with enlarged cardiac silhouette.
• In contrast to cardiac and renal disease,
uncomplicated cirrhosis is not associated with
pulmonary oedema
• Pulmonary oedema also does not occur due to
isolated hypoalbuminemia
If there is no rise in left atrial and pulmonary
capillary pressures
 Right Heart Failure
• Increased venous pressure behind the right side of
the heart increased capillary hydrostatic pressure
• Congested jugular veins
• Enlarged & tender liver
• Peripheral edema Anasarca
 Cirrhosis
• Increased venous pressure below the diseased liver
Ascites edema in the lower extremities.
• JVP is usually reduced or normal , not elevated as in
heart failure.
Can be raised if tense ascites upward pressure on
the diaphragm can increase the intrathoracic pressure

• Signs of portal hypertension

• (distended abdominal wall veins &
splenomegaly
 Renal Disease
Nephrotic Syndrome
• 2 factors:
1. sodium retention due to underlying renal disease
2. diminished transcapillary oncotic pressure gradient
• Typically- periorbital
and peripheral edema,
occasionally also ascites.
• The central venous pressure
is usually normal to high-normal
in the nephrotic syndrome.
 Renal Disease
Nephritic Syndrome
• Conditions such as in acute diffuse
glomerulonephritis and rapidly progressive
glomerulonephritis(nephritic oedema).
• There is excessive reabsorption of sodium and water
in the renal tubules via renin-angiotensin-
aldosteronemechanism.
• Mild as compared to nephrotic oedema.
• Begins in the loose tissues such as on the face
around eyes, ankles and genitalia.
 Renal Disease
Acute Tubular injury
• Acute tubular injury following shock or toxic chemicals.

• Damaged tubules lose their capacity for selective

reabsorption and concentration of the glomerular filtrate

• Resulting in increased reabsorption and oliguria.

• Excessive retention of water and electrolytes and rise in

blood urea
 Premenstrual oedema
• Retention of water and increase in weight which
occurs during or preceding menstruation.

• The etiology is poorly understood

• The edema tends to be generalized, and resolves

during a diuresis that occurs with the onset of
menses.
 Drug-induced oedema
• Direct vasodilators, such as CCB which reduce the blood
pressure activate renin-angiotensinaldosterone and
sympathetic nervous systems, both of which stimulate renal
sodium retention.
• The thiazolidinediones such as pioglitazone or rosiglitazone
stimulate sodium reabsorption by the sodium channels in the
luminal membrane of cortical collecting tubule cells
• NSAID can exacerbate edema in patients with underlying
heart failure or cirrhosis.
This effect is largely due to increased renal sodium
reabsorption in response to the inhibition of renal
vasodilatory prostaglandins.
 Cerebral oedema
• Cerebral oedema or swelling of brain is the most
threatening example of oedema.

• The mechanism of fluid exchange in the brain differs

from elsewhere in the body since there are no draining
lymphatics in the brain but instead, the function of
fluid-electrolyte exchange is performed by the blood-
brain barrier located at the endothelial cells of the
capillaries

• Can be of 3 types:
• Vasogenic oedema. This is the most common type and
corresponds to oedema elsewhere resulting from increased
filtration pressure or increased capillary permeability.

• Vasogenic oedema is prominent around cerebral contusions,

infarcts, brain abscess and some tumours.

• Grossly, the white matter is swollen, soft, with flattened gyri

and narrowed sulci. Sectioned surface is soft and gelatinous.

• Microscopically, there is separation of tissue elements by

the oedema fluid and swelling of astrocytes. The
perivascular (Virchowrobin) space is widened and clear
halos are seen around the small blood vessels
• Cytotoxic oedema. In this type, the blood-brain
barrier is intact and the fluid accumulation is
intracellular.

• The underlying mechanism is disturbance in the

cellular osmorgulation as occurs in some metabolic
derangements, acute hypoxia and with some toxic
chemicals.

• Microscopically, the cells are swollen and

vacuolated. In some situation, both vasogenic as
well as Cytotoxic cerebral oedema results e.g. in
purulent meningitis
• Interstitial oedema. This type of cerebral oedema
occurs when the excessive fluid crosses the
ependymal lining of the ventricles and accumulates
in the periventricular white matter. This mechanism
is responsible for oedema in non-communicating
hydrocephalus.
Approach to a patient presenting with
oedema
 History
• Demographic data (age ,sex)
• (dyspnea, orthopnea, edema,PND, pain abdominal distention)
• (fatigue, weakness)it’s relation to exertion.
• palpitations with or without lightheadedness.
• Anorexia ,nausea
• Drug history (thyroxine, cocaine, amphetamine)
• history of coronary artery disease or myocardial infarction,
and use of a loop diuretic .
• Family history of CAD (less than66yrs in F, less than 55yrs in M)
or unexplained death in young relative
• Social history(smoking , alcohol)
 History
• Where is the edema located?
If primary complaint is:
• SOB Left heart failure
• Ascites cirrhosis
• Peripheral edema Rt HF, pericardial disease, renal disease, local
venous or lymphatic disease
• Is there a history of any disorder (coronary disease, HTN, alcohol
abuse)??
• drug that can cause cardiac, hepatic, or renal disease?
• Is the edema intermittent or persistent?
• Intermittent edema is a common premenstrual symptom
• Associated symptoms
 Physical examination
• Pitting vs. non-pitting
• Distribution of the edema
• Localized or diffuse ?
• Periorbital ?
• Jugular veins ?
• Ascites ?
• Legs
• cardio- polumonary examination+ abdominal examination
• Stigmata of chronic liver disease
• Physical findings of heart failure
 Disorder Pulmonary oedema Central venous Ascites and/or
pressure pedal oedema
Left sided heart + Variable -
failure
Right sided heart - +
failure
Cirrhosis - or normal +

Renal disease Variable +

Nephrotic - Variable +
syndrome
Idiopathic oedema - or normal +

Venous - Normal +, oedema may be

insufficiency assymetric
 Investigations
• Chest X rays:
Cardiomegally; Pulmonary congestion; Pleural effusion.
• Echocardiography
Wall motion abnormalities; LV function; RV function; Pulmonary
hypertension.
• Abdominal US:
Liver size & morphology; Hepatic veins; Presence of ascites;
Renal morphology
• 24h urinary protein excretion

• Levels of liver enzymes, INR, albumin

• Diagnostic paracentesis
• The Serum-ascites albumin gradient (SAAG) is probably a better
discriminant than older measures (transudate versus exudate) for
the causes of ascites.
• high SAAG ("transudate") :
• Cirrhosis- 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%),
Heart failure- 3%, Hepatic Venous occlusion: Budd-Chiari
syndrome or veno-occlusive disease, Constrictive pericarditis,
Kwashiorkor (childhood protein-energy malnutrition), Nephrotic
syndrome
• low SAAG("exudate"):
• Cancer (primary peritoneal carcinomatosis and metastasis) - 10%,
Infection: TB- 2% or Spontaneous bacterial peritonitis,
Pancreatitis - 1%, Serositis, Hereditary angioedema
 Priniciples of therapy
• Reversal of the underlying disorder (if possible)

• Dietary sodium restriction

• Diuretic therapy
 Before initiating diuretics, consider the
following questions:
• When must edema be treated?

• What are the consequences of the removal of

oedema fluid?

• How rapidly should edema fluid be removed?

 When must edema be treated?
• Pulmonary edema is one of the form of
oedema that is life-threatening and requires
immediate therapy.
• In most other edematous states, removal of
the excess fluid can proceed more slowly,
since it usually is of no immediate danger to
the patient
What are the consequences of the removal
of oedema fluid?
• Sodium and water retention by the kidney is
compensatory! raises the effective circulating
volume(HF, cirrhosis).
• Diuretic therapy may have a -ve effect on systemic
hemodynamics even though it reduces the edema!!
reduction in CO +increased secretion of the
"hypovolemic" hormones
• Therefore- use diuretics, but cautiously !
• Monitor urea & creat concerntration
 How rapidly should edema fluid be
removed?
• Diuretics are administered intially fluid loss from the Intravascular
space decrease hydrostatic pressure fluid move from interstitial
space to intravascular space

• In patients with generalized edema due to heart failure, the

nephrotic syndrome, or primary sodium retention, the edema fluid
can be mobilized rapidly, since most capillary beds are involved.

• In patients with cirrhosis and ascites but no peripheral edema

300 to 500 mL/day is the maximum amount that can be mobilized

• In patients with anasarca, removal of 2 to 3 liters of edema fluid or

more in 24 hours can usually be accomplished without a clinically
significant reduction in plasma volume
 Use of Diuretics
• Start with a loop diuretic (furosemide)
• Watch for electrolyte complications:
– Hypokalemia
– Hyponatremia
– Metabolic alkalosis
• For resistant oedema- Thiazides
• Use high-dose intravenous loop diureticsspironolactone
• Use combination of diuretics to act at different
sites in the nephron
 Special considerations
• For patients with cirrhosis, spironolactone and a loop
diuretic is the preferred initial regimen
• Spironolactone contributes to the diuresis and tends
to raise K+
• For patient with NS, higher-than-usual doses of a loop
diuretic may be required because of:
• Binding of the loop diuretic by albumin in the tubular
lumen inactive
• Because transport of the diuretic into the tubular
• lumen is impaired
 ABDOMINAL PARACENTESIS

• The most efficient way

• Diagnostic & therapeutic
ABDOMINAL PARACENTESIS: Indications
New onset ascites
Hospitalization of a patient with ascites
Clinical deterioration of an inpatient or outpatient
with ascites
Fever
Abdominal pain
Abdominal tenderness
Hepatic encephalopathy
Peripheral leukocytosis
Deterioration in renal function
 ABDOMINAL PARACENTESIS:
Contraindications
• Patients with disseminated intravascular coagulation.
• Primary fibrinolysis.
• Patients with a massive ileus with bowel distension.
• The location of the paracentesis should be modified in
patients with surgical scars so that the needle is
inserted several centimeters away from the scar.
ABDOMINAL PARACENTESIS: Complications

• Ascitic fluid leak

• Bleeding
• Infection
• Mortality
 General Measures for managing Cerebral
oedema
1. Optimizing head and neck positions
2. Ventilation and oxygenation
3. Intravascular volume and cerebral perfusion
4. Seizure prophylaxis
5. Management of fever and hyperglycemia
6. Nutritional support
 CASE
• Mr.A.B., a 68 years old man, was admitted to the hospital. He
suffers from fatigue, shortness of breath on exertion, cough,
tenderness in the right upper quadrant of the abdomen and
ankle swelling.

• On examination, he was pale and his hands were cold, his

temperature was 37C, pulse 130 beats per minute and
irregular. His jugular venous was elevated and pitting edema
was present in both feet and ankles. Crepitations were
present over the lung bases. There was enlargement of the
liver beyond the costal margin that was tender.
• Heart failure is a condition in which the heart
cannot pump enough blood to the rest of the
body.
• Heart failure is usually a chronic illness, which
may get worse over time
Framingham Criteria for Dx of Heart Failure
• The Framingham criteria for the diagnosis of heart failure consists
of the concurrent presence of either 2 major criteria or 1 major
and 2 minor criteria
• Major Criteria:
• PND
• JVP
• Rales
• Cardiomegaly
• Acute Pulmonary Edema
• Gallop
• Positive hepatic Jugular reflux
• ↑ venous pressure > 16 cm H2O
• Dx of Heart Failure (cont.)
• Minor Criteria
– LL edema
– Night cough
– Dyspnea on exertion
– Hepatomegaly
– Pleural effusion
– Tachycardia 120 bpm
– Weight loss 4.5 kg over 5 days management
NYHA Classification - The
Stages of Heart Failure
Investigations
 Treatment of heart failure
• Treatment focuses on improving the symptoms and
preventing the progression of the disease.

Diet and Life style Pharmacological

modification management
 Diet and lifestyle measures
• Education in term of explaining the nature of the disease and
treatment.
• Moderate physical activity, when symptoms are mild or
moderate; or bed rest when symptoms are severe.
• Weight reduction; as obesity is a risk factor for heart failure
and left ventricular hypertrophy
• Sodium restriction 60–100 mmol total daily intake. More
severe restrictions may be required in severe CHF.
• Fluid restriction should be limited to 1.5 L daily or less in
patients with hyponatremia.
• Influenza and pneumococcal vaccination should be
considered.